Pulmonary Artery Occlusion Research Articles

Exercise right heart catheterization predicts outcome in asymptomatic degenerative aortic stenosis.

Degenerative aortic stenosis (DAS) is the most frequent valvular heart disease. It remains unclear how to identify asymptomatic DAS patients with normal left ventricular ejection fraction who have a high probability of event occurrence and would thus benefit from early intervention. Here, we describe a protocol for exercise hemodynamics in true asymptomatic patients with moderate or severe DAS and assess the prognostic value of the data obtained in this population. This study involved a prospective single-centre registry of consecutive asymptomatic patients with moderate or severe DAS. Patients underwent cardiopulmonary exercise testing to confirm symptom absence during exercise and then right heart catheterization (RHC) at rest and during exercise. Events were defined as death, surgical aortic valve replacement, or transcatheter aortic valve implantation according to clinical guidelines. Thirty-three patients underwent baseline and exercise RHC. The mean aortic valve area was 1.08 cm2 and the aortic gradient was 39mmHg. The mean pulmonary artery pressure was 21mmHg with a pulmonary artery occlusion pressure of 14mmHg and cardiac output of 5.6 L/min. The mean pulmonary artery pressure at peak exercise was 34mmHg. After a mean follow-up of 27 months, 8 patients experienced an event (24%). There were no differences in baseline variables, aortic valve area, or cardiopulmonary exercise testing parameters between the event and event-free groups. Patients with an event did not have higher pulmonary or filling pressures after peak exercise but had lower pulmonary artery oxygen saturation on effort (median, 48% vs 57%, P=.03). Exercise RHC is feasible and safe in this population. Peak pulmonary artery oxygen saturation might identify patients with increased risk of serious adverse events.

The Left Pneumonectomy Combined with Monocrotaline or Sugen as a Model of Pulmonary Hypertension in Rats.

In this protocol, we detail the correct procedural steps and necessary precautions to successfully perform a left pneumonectomy and induce PAH in rats with the additional administration of monocrotaline (MCT) or SU5416 (Sugen). We also compare these two models to other PAH models commonly used in research. In the last few years, the focus of animal PAH models has moved towards studying the mechanism of angioproliferation of plexiform lesions, in which the role of increased pulmonary blood flow is considered as an important trigger in the development of severe pulmonary vascular remodeling. One of the most promising rodent models of increased pulmonary flow is the unilateral left pneumonectomy combined with a "second hit" of MCT or Sugen. The removal of the left lung leads to increased and turbulent pulmonary blood flow and vascular remodeling. Currently, there is no detailed procedure of the pneumonectomy surgery in rats. This article details a step-by-step protocol of the pneumonectomy surgical procedure and post-operative care in male Sprague-Dawley rats. Briefly, the animal is anesthetized and the chest is opened. Once the left pulmonary artery, pulmonary vein, and bronchus are visualized, they are ligated and the left lung is removed. The chest then closed and the animal recovered. Blood is forced to circulate only on the right lung. This increased vascular pressure leads to a progressive remodeling and occlusion of small pulmonary arteries. The second hit of MCT or Sugen is used one week post-surgery to induce endothelial dysfunction. The combination of increased blood flow in the lung and endothelial dysfunction produces severe PAH. The primary limitation of this procedure is that it requires general surgical skills.

A case of lung cancer associated with partial anomalous pulmonary venous connection in the lobe that should be preserved - The efficacy of a selective pulmonary arterial occlusion test -

A case of lung cancer associated with partial anomalous pulmonary venous connection in the lobe that should be preserved - The efficacy of a selective pulmonary arterial occlusion test -

Foramen ovale blood flow and cardiac function after main pulmonary artery occlusion in fetal sheep.

What is the central question of this study? At near-term gestation, foramen ovale blood flow accounts for a significant proportion of fetal left ventricular output. Can the foramen ovale increase its volume blood flow when right ventricular afterload is increased by main pulmonary artery occlusion? What is the main finding and its importance? Foramen ovale volume blood flow increased during main pulmonary artery occlusion. However, this increase was attributable to an increase in fetal heart rate, because left ventricular stroke volume remained unchanged. These findings suggest that the foramen ovale has a limited capacity to increase its volume blood flow. The foramen ovale (FO) accounts for the majority of fetal left ventricular (LV) output. Increased right ventricular afterload can cause a redistribution of combined cardiac output between the ventricles. To understand the capability of the FO to increase its volume blood flow and thus LV output, we mechanically occluded the main pulmonary artery in seven chronically instrumented near-term sheep fetuses. We hypothesized that FO volume blood flow and LV output would increase during main pulmonary artery occlusion. Fetal cardiac function and haemodynamics were assessed by pulsed and tissue Doppler at baseline, 15 and 60min after occlusion of the main pulmonary artery and 15min after occlusion was released. Fetal ascending aorta and central venous pressures and blood gas values were monitored. Main pulmonary artery occlusion initially increased fetal heart rate (P<0.05) from [mean(SD)] 158(7) to 188(23)beatsmin-1 and LV cardiac output (P<0.0001) from 629(198) to 776(283)mlmin-1 . Combined cardiac output fell (P<0.0001) from 1524(341) to 720(273)mlmin-1 . During main pulmonary artery occlusion, FO volume blood flow increased (P<0.001) from 507(181) to 776(283)mlmin-1 . This increase was related to fetal tachycardia, because LV stroke volume did not change. Fetal ascending aortic blood pressure remained stable. Central venous pressure was higher (P<0.05) during the occlusion than after it was released. During the occlusion, fetal pH decreased and increased. Left ventricular systolic dysfunction developed while LV diastolic function was preserved. Right ventricular systolic and diastolic function deteriorated after the occlusion. In conclusion, the FO has a limited capacity to increase its volume blood flow at near-term gestation.

EFFECTS OF A SUPPLEMENTAL ETORPHINE DOSE ON PULMONARY ARTERY PRESSURE AND CARDIAC OUTPUT IN IMMOBILIZED, BOMA-HABITUATED WHITE RHINOCEROS ( CERATOTHERIUM SIMUM): A PRELIMINARY STUDY.

The effects of etorphine on the pulmonary vascular system of white rhinoceros ( Ceratotherium simum) have not been described and could play a role in the severe hypoxemia that develops after immobilization with etorphine-based drug combinations. Characterization of these effects requires measurement of pulmonary vascular pressures and cardiac output (CO). To refine a technique for pulmonary arterial catheterization, five boma-habituated white rhinoceros (three females and two males weighing 1,012-1,572 kg) were immobilized by remote injection with etorphine plus azaperone followed by butorphanol. This afforded the opportunity to perform a pilot study and acquire preliminary measurements of pulmonary arterial pressure (PAP) and CO before and after supplemental etorphine given intravenously. Ultrasonographic guidance was used to insert a sheath introducer into a linguofacial branch of a jugular vein. A 160-cm-long pulmonary artery catheter with a balloon and thermistor was then passed through the introducer and positioned with its tip in the pulmonary artery. It was not long enough to permit wedging for measurement of pulmonary artery occlusion pressure. Mean PAP was 35 mm Hg (minimum, maximum 32, 47 mm Hg) and increased ( P = 0.031) by 83% (28, 106%) after supplemental etorphine. Thermodilution CO was 120 L/min (92, 145 L/min) and increased 27% (3, 43%) ( P = 0.031). Heart rate was 100 (88, 112) beats/min and increased 20% (4, 45%) ( P = 0.031), whereas arterial partial pressure of oxygen was 35 mm Hg (30, 94 mm Hg) and decreased 47% (20, 72%) ( P = 0.031). The cardiovascular observations could result from etorphine-induced generalized sympathetic outflow, as has been reported in horses. Further studies of etorphine in isolation are needed to test this suggestion and to discern how the changes in pulmonary vascular pressures and blood flow might relate to hypoxemia in etorphine-immobilized white rhinoceros.

CB2-deficiency is associated with a stronger hypertrophy and remodeling of the right ventricle in a murine model of left pulmonary artery occlusion

AimsPulmonary hypertension (PH) leads to right ventricular (RV) adaptation and remodeling and has deleterious long-term effects on RV function. The endocannabinoid receptor CB2 has been associated with protective effects in adaptation and remodeling of the left ventricle after ischemia. Therefore, we investigated the role of CB2 receptor in RV adaptation after occlusion of the left pulmonary artery (LPA) in a murine model. Main methodsC57/Bl6 (WT)- and CB2 receptor-deficient (Cnr2−/−)-mice underwent paramedian sternotomy and LPA was occluded using a metal clip. Right heart hemodynamic study (Millar®) preceded organ harvesting for immunohistochemistry and mRNA analysis 7 and 21 days (d) post-occlusion. Key findingsLPA occlusion led to higher RV systolic pressure in Cnr2−/−-hearts, while hemodynamics were comparable with WT-hearts after 21d. Cnr2−/−-hearts showed higher macrophage infiltration and lower interleukin-10 expression after 7 d, but otherwise a comparable inflammatory mediator expression profile. Cardiomyocyte-hypertrophy was stronger in Cnr2−/−-mice, presenting with higher tenascin-C expression than WT-hearts. Planimetry revealed higher collagen area in Cnr2−/−-hearts and small areas of cardiomyocyte-loss. Surrounding cardiomyocytes were cleaved caspase-3- and TUNEL positive in Cnr2−/−-hearts. This was associated by maladaptation of myosin heavy-chain isoforms and lower reactive oxygen scavenger enzymes induction in Cnr2−/−-hearts. We found comparable morphological changes in both lungs between the two genotypes. SignificanceLPA occlusion led to increased systolic pressure and adaptation of RV in CB2-deficient mice. CB2 receptor seems to modulate RV adaptation through expression of contractile elements, reactive oxygen scavenger enzymes, and inflammatory response in order to prevent cardiomyocyte apoptosis.

OC44 VENTRICULAR TACHYCARDIA SURGICAL ABLATION IN REPAIRED TETRALOGY OF FALLOT PATIENTS

Background and Aim: Arrhythmias are the main causes of mortality in repaired TOF patients and ventricular tachycardia, due to abnormal electrical conduction near patches and surgical incisions, is refractory to medical therapy. The aim of the study is to evaluate the effectiveness of surgical ventricular RF ablation during pulmonary valve replacement. Methods: 20 patients (median age 37,5 y) in 2004–2013 underwent re-operation for symptomatic pulmonary valve regurgitation with RF ablation, 28 (16–39) years after first repair. Inducible VT was demonstrated during preoperative electrophysiological study in all. Median QRS was 178 (100–268) ms. Right ventricular dilation and dysfunction were present in all, with moderate-to-severe tricuspid regurgitation in 20%. Eleven patients showed spontaneous ventricular arrhythmia, 5 had preoperative ICD, and one presented out-of-hospital cardiac arrest. Surgical ablation of the slow-conducting isthmus between the VSD patch and the pulmonary annulus was performed with linear RF lesions. All patients underwent clinical evaluation, echocardiography and Holter-ECG at 1-3-6 months together with electrophysiological study after 6 months. Results: 16 patients underwent RVOT reduction and 4 TV repair. Median follow-up of 6.5 years was complete. 1 patient with pulmonary artery occlusion died on V-V ECMO for respiratory failure. No late mortality was observed. Residual inducible VT was present in 3/19 patients, whom received ICD as primary prevention. Freedom from ventricular arrhythmia was respectively 94% and 89.5% at 1 and 5 years of follow-up. Conclusion: Pulmonary regurgitation and ventricular dysfunction are correlated with SCD. Ablation of slow-conducting isthmus between the pulmonary valve and VSD patch prevents ventricular arrhythmias.

Long-Term Outcome of Oncologic Right Pulmonary Artery Occlusion

Long-Term Outcome of Oncologic Right Pulmonary Artery Occlusion

GW29-e1126 Chronic Thromboembolic Pulmonary Hypertension(CTEPH): Outcomes of Surgical Effect in Patients with Unilateral Main Pulmonary Artery Occlusion

To summarize the clinical characteristics and the effect of pulmonary endarterectomy(PEA) in CTEPH patients with unilateral main pulmonary artery occlusion. Of 160 CTEPH patients operated between January 2004 and March 2018 at our center,13(8.1%) had complete main pulmonary artery occlusion.

MYELOPROLIFERATIVE NEOPLASMS AND PULMONARY HYPERTENSION: AN ASSOCIATION REDEFINED

SESSION TITLE: Pulmonary Vascular Disease 2 SESSION TYPE: Original Investigation Posters PRESENTED ON: 10/10/2018 01:00 PM - 02:00 PM PURPOSE: The association between pulmonary arterial hypertension (PAH) and myeloproliferative neoplasms (MPNs) is described for each of the 4 distinct MPN subtypes; essential thrombocythemia (ET), polycythemia vera (PCV), primary myelofibrosis (PMF) and chronic myelogenous leukemia (CML). These associations are largely based on small studies, often using echocardiographic parameters as the basis for PH diagnosis. No study has closely evaluated the hemodynamic features of patients with CMPD associated PH. We sought to characterize the hemodynamic features of this cohort by right heart catheterization and compare those to echocardiogram (TTE) findings. We also evaluated whether hemodynamic differences exist among distinct MPN subtypes. METHODS: This single-center retrospective analysis included patients over 18 years old with an MPN and a documented right heart catheterization (RHC) between the years of 2004 and 2017. The MPN subtype was determined by ICD-9 code. Clinical characteristics nearest the time of right heart catheterization were recorded. PH was diagnosed by TTE if right ventricular systolic pressure (RVSP) was >35mmHg and by RHC if the mean pulmonary artery (PA) pressure was >25mmHg and PA occlusion pressure (PAOP) <15mmHg. Linear regression was used to determine association between TTE and RHC RVSP. One-way ANOVA was used to determine hemodynamic differences between CMPD subtypes. RESULTS: 74 subjects met inclusion criteria. They were predominantly male (58.1%) and Caucasian (87.8%). Median age was 63 years (+/-13yrs). MPN subtypes included PCV (35.1%), ET (24.3%), CML (22.9%), and PMF (16.2%). RHC indices showed mean PA pressure 36.3 (+/- 12 mmHg), PA occlusion pressure 18 (+/-7.4 mmHg), and cardiac output 5.3 (+/- 1.8 l/min). Median time between RHC and TTE was 13 months (IQR 2.5-39). The mean RVSP derived by TTE was 60 (+/-22) mmHg). This did not differ from RHC derived mean RVSP of 57 (+/-19) mmHg. By TTE, 90.6% of patients had PH. Although 84% of patients had mean PA pressure >25mmHg on RHC, a majority of those had PAOP > 15mmHg. Only 28.5% of subjects met full criteria for PAH by RHC. No differences in RVSP (on TTE) or hemodynamic indices were identified between subtypes of MPN. CONCLUSIONS: Although echocardiographic evaluation closely reflects PA catheter derived RVSP, many of these patients demonstrate pulmonary venous hypertension. Thus, echo may not be a reliable substitution for RHC to study or diagnose PAH in this cohort. Among patients with MPN and PAH, hemodynamics do not differ by MPN subtype. CLINICAL IMPLICATIONS: Echo while useful to evaluate PH in patients with MPN, is not a reliable alternative to diagnose PAH and echo criteria likely significantly overestimate the actual prevalence of PAH in clinical practice. DISCLOSURES: Advisory Committee Member relationship with Bayer Please note: $5001 - $20000 Added 03/04/2018 by Neal Chaisson, source=Web Response, value=Consulting fee Speaker/Speaker's Bureau relationship with Gilead Please note: $5001 - $20000 Added 03/04/2018 by Neal Chaisson, source=Web Response, value=Consulting fee Advisory Committee Member relationship with Actelion Please note: $5001 - $20000 Added 03/04/2018 by Neal Chaisson, source=Web Response, value=Consulting fee Consultant relationship with American College of Physicians Please note: $1001 - $5000 Added 03/04/2018 by Neal Chaisson, source=Web Response, value=Honoraria Removed 03/04/2018 by Neal Chaisson, source=Web Response Consultant relationship with Schlesimger Please note: $1-$1000 Added 03/04/2018 by Neal Chaisson, source=Web Response, value=Consulting fee Removed 03/04/2018 by Neal Chaisson, source=Web Response Consultant relationship with Putnam Associates Please note: $1-$1000 Added 03/04/2018 by Neal Chaisson, source=Web Response, value=Consulting fee Removed 03/04/2018 by Neal Chaisson, source=Web Response No relevant relationships by Nauman Khan, source=Web Response

Endovascular treatment of acute pulmonary embolism

Thromboembolism of pulmonary artery is life-threatening condition due to acute right ventricle failure and cardiogenic shock. System thrombolysis is the main way of reperfusion in massive pulmonary embolism with a very high risk of fatal hemorrhage complications. There is a popular revascularization method in two last decades such as endovascular treatment. It allows to recover the blood flow into occluded pulmonary arteries up to three weeks after confirmed embolism episode and to decrease major bleeding risks. Now trials corroborate the high efficacy and safety of interventional treatment the usage of which would allow to improve prognosis in massive pulmonary embolism.

Levosimendan in patients with cardiogenic shock complicating myocardial infarction: A meta-analysis

PurposeCardiac shock is the leading cause of death in patients with acute myocardial infarction. The objective of this systematic review and meta-analysis was to evaluate whether levosimendan, compared to any type of control, is associated with improved clinical outcomes in patients with cardiogenic shock complicating myocardial infarction. Materials and methodsThe PubMed, EMBASE, Cochrane Central Register, and China National Knowledge Information databases were searched for pertinent studies published up until 1 May 2016. Randomized and non-randomized clinical trials comparing levosimendan to standard therapy or placebo, in adult patients with cardiogenic shock complicating myocardial infarction, and reporting at least one outcome of interest were included. The primary outcome was mortality, whereas secondary outcomes were length of ICU stay, SOFA score, cardiac index (CI), cardiac power index (CPI), ejection fraction (EF), end-systolic volume (ESV), mean blood pressure (MBP), pulmonary arterial pressure (PAP), mixed venous oxygen saturation (SvO2), pulmonary artery occlusion pressure (PAOP) and glomerular filtration rate (GFR). We pooled risk ratio (RR) and 95% confidence interval (CI) using fixed and random effects models. ResultsThirteen studies comprising a total of 648 patients were included in the analysis. There was a nonsignificant reduction in mortality with levosimendan compared to the controls (RR=0.82 [0.65–1.01], P for effect=0.07, I2=0%). In the levosimendan group PAP and ESV were significantly reduced, while CI, CPI, EF, MBP and SvO2 were significantly increased. No differences in SOFA score, ICU days, PAOP or GFR were noted. ConclusionsLevosimendan can improve hemodynamic parameters and cardiac function when compared with a control group, with no evidence of benefit in terms of survival.

C albicans FH binding molecule Hgt1p, a low glucose induced membrane protein trafficked to the cell wall impairing phagocytosis

We present the case of a patient with symptomatic ventilation-perfusion mismatch due to mixed pulmonary arterial and venous obstruction after partial right lung resection for non-small cell lung cancer. Non-invasive imaging suggested complete occlusion of the right lower lobe pulmonary artery, but we were able to successfully percutaneously recanalize the vessel and improve his symptoms and quality of life.

Dual-Energy CT Pulmonary Angiography: Quantification of Disease Burden and Impact on Management

Computed tomography pulmonary angiography (CTPA) has become the imaging modality of choice for patients with suspected pulmonary embolism (PE). Post-processing techniques currently available for dual-energy CT pulmonary angiography (DE-CTPA) enhance image quality and provide additional value in the diagnosis of PE. The objective of this article is to summarize these recent developments and discuss the appropriate use of DE-CTPA post-processing applications. DE-CTPA post-processing applications enable reconstruction of virtual monoenergetic images (VMI) and color-coded iodine-perfusion maps to increase contrast conditions and visualize lung perfusion defects in case of embolic occlusion of pulmonary arteries. Both techniques revealed a superior diagnostic performance for the detection of pulmonary emboli and assessment of the pulmonary perfusion compared to the standard image reconstructions. DE-CTPA is a well-established method for excluding or diagnosing PE. Continued developments in DE-CTPA post-processing techniques improve patient management and allow for a quantification of disease burden.

Abstract 250: Pulmonary Hypertension Induced by 15-HETE is Reverse by Apoai Mimetic Peptide 6f Administration

Pulmonary arterial hypertension (PAH) is characterized by pulmonary arterial occlusion leading to increased pulmonary arterial pressure. Recently, a growing body of evidence demonstrated a robust increase in oxidized lipids, including 15-hydroxyeicosatetraenoic acids (15HETE), in the lungs and plasma of PAH patients and animal models of pulmonary hypertension (PH). Recently, our group demonstrated that 15HETE induce PH. Nonetheless, the precise mechanism by which 15HETE participates in PH development remains elusive. In order to investigate this mechanism, we fed wild type mice with a diet rich in 15HETE and examine whether ApoA-I mimetic peptide can rescue PH induced by 15HETE. Methods: Wild type male mice (C57BL/6) were fed for 3 weeks for 3 weeks with regular chow (n=16-21 mice/group), 15HETE (5μg/day), 15HETE diet supplemented with either empty vector or 6F for the last week of 15HETE diet. PH development was assessed every week via serial echocardiography. Right ventricular systolic pressure (RVSP) was measured via heart catheterization. RV hypertrophy index (RV/[IVS+LV]) was measured. Lung morphology and lipid accumulation were assessed using H&amp;E and Oil red O staining. Results: Echocardiography revealed the first sign of PH as early as one week after starting 15HETE diet and a significant decrease in the pulmonary arterial acceleration time (PAAT) after 2 weeks of treatment (16.6±1.9 vs. 20.6±1.4 msec, p&lt;0.05). At the end of three weeks, mice on 15HETE diet had significantly higher RVSP (31.3±1.1 vs. 38.4±2.3 mmHg, p&lt;0.05) and RV hypertrophy index (0.26 ± 0.02 vs. 0.33 ±0.02, p&lt;0.05). This increased pressure was concomitant with a significant increase in pulmonary arteriolar thickness in mice on 15-HETE diet compared to regular diet (35.1±0.8 vs 53.4±1, p&lt;0.05). Furthermore, these WT mice did not develop atherosclerosis as there was no detectable plaque in aorta of the mice on 15HETE diet. At the end of three weeks mice treated with 6F showed a PAAT similar to control value(19±0.5 msec) concomitant with a significantly lower RVSP than mice fed with 15HETE +empty vector (33.6 ±5.7 vs 40.3±4.6, p&lt;0.05). Conclusion: Our data demonstrates that APOA-I mimetic peptide 6F is able to rescue pre-exisiting PH induced by 15-HETE diet in wild type mice.

The Person Behind the Inventor of the Heart-Lung Machine: John H. Gibbon Jr, MD (1903-1973).

The Person Behind the Inventor of the Heart-Lung Machine: John H. Gibbon Jr, MD (1903-1973).

Triple-tyrosine kinase inhibition attenuates pulmonary arterial hypertension and neointimal formation

The present study examined the effects of simultaneous inhibition of vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF) and fibroblast growth factor (FGF) receptor signaling with BIBF1000, a novel triple tyrosine kinase inhibitor on preventing and reversing the progression of severe pulmonary arterial hypertension (PAH) in an experimental model in rats. Left pneumonectomized male Wistar rats were injected with monocrotaline to induce PAH. Treatment with BIBF1000 from day 1 to day 21 after monocrotaline injection attenuated PAH development, as evidenced by lower values for pulmonary artery pressure (mPAP), right ventricular pressure (RVSP), pulmonary arterial neointimal formation, and the ratio of right ventricular weight to left ventricular and septum weight [RV/(LV+S)] on day 21 compared to control rats. Treatment with BIBF1000 from day 21 to day 42 after monocrotaline injection reversed established PAH as shown by normalized values for mPAP and RVSP, RV/(LV+S) ratio, pulmonary arterial occlusion scores, levels of heart and lung fibrosis, as well as improved survival. Treatment with BIBF1000 reduced inflammatory cell recruitment in bronchoalveolar lavage and lung tissues, reduced CD-68 positive macrophages and expression of proliferating cell nuclear antigen in the perivascular areas, and reduced TNF-α and growth factor productions, and inhibited the phosphorylation of AKT and GSK3β in lungs. In addition, BIBF1000 inhibited pulmonary artery smooth muscle cells migration and proliferation from rat pulmonary artery explant cultures. Simultaneous inhibition of VEGF, PDGF, and FGF receptor signaling by BIBF1000 prevents and reverses the progression of severe pulmonary arterial hypertension and vascular remodeling in this experimental model.

Percutaneous intervention for diffuse pulmonary arteriovenous malformations by occlusion of large lobar pulmonary arteries

We present a case of an 8-year-old girl with bilateral, diffuse, lower lobe pulmonary arteriovenous malformations (PAVMs). These were initially treated by selective embolisation of the feeder arteries with coils and vascular plugs. Due to unsatisfactory results (persistent cyanosis and diffuse residual PAVMs), prolonged procedure time, high contrast dose and the fact that she was declined surgical resection by cardiothoracic surgery as she was perceived to be a high anaesthetic risk and surgical resection was presumed to be complex; a staged approach for occlusion of the left and right lower lobar pulmonary arteries with large vascular plugs was chosen.

Relationship of inferior vena cava collapsibility to ultrafiltration volume achieved in critically ill hemodialysis patients.

BackgroundUltrasound (US) assessment of intravascular volume may improve volume management of dialysis patients. We investigated the relationship of intravascular volume evaluated by inferior vena cava (IVC) US to net volume changes with intermittent hemodialysis (HD) in critically ill patients.MethodsA retrospective cohort of 113 intensive care unit patients in 244 encounters had clinical assessment of intravascular volume followed by US of respiratory/ventilatory variation of IVC diameter, and had HD within 24 h. IVC collapsibility index (IVC CI)=(IVCmax–IVCmin)/IVCmax*100%. Volume management was guided by clinical data plus IVC US findings. Intradialytic hypotension (IDH) was categorized by severity from none to inability to tolerate HD.ResultsLinear regression correlating n-weighted proportions of encounters achieving net volume removal of ≥0.5 L, ≥1.0 L, ≥1.5 L, and ≥2.0 L strongly correlated across the range of IVC CI (R2=0.87–0.64). Sensitivity and specificity analysis showed IVC CI was a better predictor than IVCmax of achieving net ultrafiltration (UF) volumes. Mean central venous pressure, pulmonary artery occlusion pressure, and cardiac output were poor predictors by logistic regression and receiver operating curve analyses. IVC CI <20% was the approximate optimal cutoff for achieving ≥0.5 L to ≥2.0 L net UF volumes. Net volume change achieved tended to be less than recommended and may have been limited by the development of IDH. Severity of IDH did not correlate with UF rate in mL/kg/h. χ2 analysis showed pre-US clinical intravascular volume assessments had poor concordance with IVC CI categories.ConclusionIVC US may be a useful tool for predicting whether critically ill patients will achieve volume removal with HD.

Effect of dexmedetomidine on renal injury induced by lung ischemia/reperfusion in mice

To evaluate the effect of dexmedetomidine(Dex) on renal injury induced by lung ischemia/reperfusion(I/R) in mice. Fifty healthy SPF male C57BL/6J mice, weighing 20 g~24 g,aged 8~10 weeks,were randomly divided into five groups(n=10 each):sham operation group(sham group),lung ischemia/reperfusion group(I/R group), lung ischemia/reperfusion and normal saline group (NS group), dexmedetomidine group(Dex group), dexmedetomidine and atipamezole group (DA group). Lung ischemia/reperfusion model was established by occlusion of the left pulmonary artery for 30 min followed by 180 min reperfusion in mice. In Dex and DA groups, dexmedetomidine 20 μg/kg and dexmedetomidine 20 μg/kg plus atipamezole 250 μg/kg were injected intraperitoneally respectively at 30 min before establishment of the model, isopyknic normal saline instead of Dex were injected intraperitoneally in NS group. After the experiment the mice were killed and plasma IL-1 beta and tumor necrosis factor α(TNF-α) concentration were detected by ELISA; the renal tissues were harvested to observe ultra structure under electron microscope. Compared with sham group, the concentrations of IL-1β and TNF-α in other groups were increased significantly and the structure damages of renal tissues observed under electron microscope in other groups were more serious than those of sham group. Compared with I/R group, NS groups and DA group, the concentrations of IL-1β and TNF-α in Dex group were significantly lower(P<0.05)and the structure damages of renal tissues observed under electron microscope in Dex group were slighter. Dexmedetomidine pretreatment can attenuate renal injury induced by lung ischemia/reperfusion and the mechanism may be related to inhibition of inflammatory responses.